A fundamental goal of biological psychiatry should be the separation of symptoms from syndromes. It is clear, for example, that
'headache' is not an appropriate diagnostic category. You cannot
use it to define the treatment of the underlying disorder giving rise
to the symptom. Nor is the regular decrease in headache symptoms
produced by aspirin or paracetamol evidence for common aetiology
of the causes of headache or for an 'analgesic insufficiency' as the
primary cause of headache.

This problem is particularly acute with mood disorders. In the
case of depression, which at first blush seems more coherent as an
entity than the spectrum of 'anxiety disorders',

'in the DSM-III the “choice principle” was introduced. For the
diagnosis of a particular syndrome the presence of X out of a
list of Y symptoms suffices, no matter which ones. Hence the
various disorders that are distinguished are symptomatologically
ill defined. In fact, many different syndromes carry the same
designation: major depression and dysthymia.… The utility of the
… discrete diagnostic entities characterized by multiple criteria …
is questionable. Our studies at least have failed to validate them.…
Another fundamental shortcoming … is the lack of an aetiological
axis [since] with today's methodologies, one can arrive at an
aetiological hypothesis with no less reliability as one can regarding
the presence or absence and severity of particular psychopathological
symptoms.… Another [problem] is that of [classification in the
presence of] comorbidity … For the diagnosis of major depression,
psychotic and organic conditions have to be ruled out. The diagnosis
of generalized anxiety disorder cannot be made in the presence of a
mood disorder.

This principle is not applicable in biological psychiatry. One can
and should not simply discart [sic] the possibility that a biological
variable observed in a psychotic condition is linked to a concurrent
depression, or one found in depression is in fact related to an anxiety
disorder.…

For [these] reasons I consider these concepts unsuited for [mood
disorder] research, particularly biological research, requiring as it
does well-defined and assessable diagnostic concepts.'

Van Praag (1995, p. 270)

The problem of comorbidity may be even more acute in the
diagnosis of anxiety disorders. For example, panic and obsession, as disorders, may well have no necessary connection to anxiety
as such. Rather, each may be an indirect cause of, essentially
'normal', anxiety when they occur (as unexpected, uncontrollable
and bizarre events) in someone with a pre-existing sensitivity
to threatening events. Conversely, both panic and obsession can
occur as a simple, non-pathological, consequence of high levels of
anxiety. Even this anxiety need not be pathological—consider the
obsessive behaviour of a parent with a young and extremely mobile
child at an airport.

Syndrome identification faces two additional problems. First,
is a lack of connection between cause and treatment. A purely
cognitively mediated post-traumatic stress disorder can nonetheless
result in brain damage and require pharmacological treatment. Panic
attacks resulting from a neural disturbance may be best treated
psychologically—resolving the anxiety-related problems engendered by the panic attacks without completely eliminating the latter
(Franklin, 1990). Other exclusion criteria, such as the exclusion by
'DSM-III-R [of] persons with socially phobic symptoms secondary
to axis III conditions … [such as] disfiguring or disabling conditions [can lack] empirical basis.…[and cause] a patient group
[to be] overlooked with regard to treatment options' (Oberlander,
Schneier and Liebowitz, 1994).

A final problem for diagnosis is that the grouping of 'anxiety
disorders' as a single class in DSM-III, DSM-IIR and DSMIV seems inappropriate from the point of view of pharmacology
or preclinical analysis of brain systems. These suggest that the
different symptomatologies and therapeutic responses of patients
presenting with 'anxiety disorders' reflects a confusion of diagnostic
categories. Diagnoses should, but currently do not, reflect the
primary brain systems that are dysfunctional in any particular case.
Symptomatology must often reflect the brain systems, whether
functional or dysfunctional, that have extremes of activity. For both
these reasons, brains systems will be the focus of the next section.

The most significant aminergic neurotransmitter systems for
anxiety and the conventional grouping of anxiety disorders are
the monoamines serotonin and noradrenaline. As discussed in the
section entitled 'The Neuropsychology of the aminergic systems'
basic research implicates them as modulators of the entire defense
system with a clear contribution to anxiety — in the sense that
this can be distinguished from fear (Blanchard et al., 1988, 1991,
1997). Drugs that manipulate them have therapeutic effects that
usually span several of the different types of anxiety disorder
(den Boer et al., Chapter XIX-13). Finally, disturbances of their
metabolism appear to play a significant role in the generation
of anxiety disorders (see below). A weaker case can, also, be
made for dopamine. The preclinical review below will also include
consideration of acetylcholine because, although not a monoamine,
it shares many of the anatomical and functional features of the
monoamines.

The primary conclusion is that the success or failure of treatment
with a particular drug is likely to reflect the secondary impact of
alteration in monoamines on primary brain systems more often than
an original disturbance of monoamines was the primary basis of the
symptomatology.

THE NEUROPSYCHOLOGY OF ANXIETY

The view of the neuropsychology of anxiety disorders in this
chapter is justified at great length in Gray and McNaughton

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